oxygen delivery jenny boyd, md. case #1 12 mo male with a history of truncus arteriosus type i s/p...
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Oxygen DeliveryJenny Boyd, MD
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Case #1 12 mo male with a history of truncus
arteriosus type I s/p repair with placement of a RV-PA conduit as a newborn who is now s/p conduit replacement. Patient is being admitted to the PCCU post-operatively.
What are the goals of our care?
Images from American Heart Association
12 mo male who just had heart surgery and is very sick. We have to take care of him until 7AM when the morning crew arrives.
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Care of the PCCU Patient
2 main goals of critical care:
Ensure adequate oxygen delivery!
Buy time!
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Why Is Oxygen Important? Used in cellular respiration
Needed for energy production by cells and tissues
GLYCOLYSISKREB’S CYCLE
+ELECTRON TRANSPORT
Pyruvate
Glucose Oxygen2 ATP
34 ATP
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Case #1 (cont.) Initial assessment: PERRL, clear BS
bilaterally, RRR, soft belly, warm extremities, well-perfused, 2+ pulses, brisk cap refill.
Initial CXR looks good, all tubes and lines in expected places.
Initial ABG: pH 7.32, pCO2 52, pO2 142, BE -0.2, lactate 3.9 (nl <2) Initial elevation of lactate very common post-
bypass, should resolve within 4 hours
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Case #1 (cont.) Over the next few hours, patient is
hemodynamically stable with good perfusion, decent UOP and minimal bleeding from surgical site.
Repeat ABGs are normal except the lactate rises from 3.9 4.4 5.1
Are you worried? Is an elevated lactate harmful?
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Where Does Lactate Come From?
GLYCOLYSISKREB’S CYCLE
+ELECTRON TRANSPORT
Pyruvate
Glucose Oxygen2 ATP
34 ATP
Lactate
So, why is our patient’s lactate elevated?
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Oxygen Delivery O2 delivery dependent on cardiac output and
O2 content of the blood
O2 content is primarily due to hemoglobin saturation with little contribution of dissolved O2 in blood
CCaaOO22 = (S = (SaaOO22* Hb * 1.34)+(0.003 * P* Hb * 1.34)+(0.003 * PaaOO22))
DODO22 = = CCaaOO22 ** Q Q. .
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Oxygen Delivery (cont.) From previous equations, we can simplify to:
So, there are 3 reasons for poor O2 delivery:
1) anemic anoxemia (low Hgb)
2) anoxic anoxemia (low SaO2)
3) stagnant anoxemia (low Q).
O2 Delivery ≈ Hgb x SaO2 x Q.
How much O2 delivery does our patient need?
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Oxygen Consumption Goal: O2 delivery > O2 consumption
Adequate O2 delivery may become insufficient if tissue O2 consumption increases! Fever increases O2 consumption 10% per degree
Agitation can increase O2 consumption by 40%
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Back to the Patient! Due to the elevated lactate, we minimize O2
consumption by ensuring our patient is afebrile and well sedated. However, our next lactate has risen to 7.0.
What’s wrong with our patient? Anemic? Low sats? Low cardiac output?
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Our Patient (cont.) Since return from the OR, our patient’s Hgb
has been > 10 and SaO2 has been >95%
How do we know what our cardiac output is? What determines cardiac output?
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Measuring Cardiac Output Thermodilution
Need cardiac catheterization
Echocardiography Need an echocardiographer Shortening fraction
Surrogate markers Oxygen extraction
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Oxygen Extraction Measure O2 consumption by looking at O2
extraction: SaO2 – SvO2
Should be ~20 - 30 mmHg Need arterial line and right atrial line
Increased O2 extraction can be due to increased O2 consumption (hungry mouths) or decreased O2 delivery (not enough food)
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Regional Oxygen Extraction NIRS (Near-Infrared
Spectroscopy) Monitoring Measures organ-
specific oxygen extraction Kidney – Surrogate for
cardiac output ≈ SaO2 – 15
Brain – Because the brain is important! ≈SaO2 – 30
Image from Children’s Hospital of Wisconsin
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Understanding Cardiac Output (Q) Q = Heart Rate x Stroke Volume
What determines stroke volume? Preload Contractility Afterload
.
.
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Frank-Starling Curve Increasing preload
increases myosin-actin overlap, resulting in increased stroke volume
Increasing contractility increases stroke volume for a given preload
Increasing afterload decreases stroke volume for a given preload Preload
Stro
ke V
olum
e
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Increasing cardiac output (Q) Remember: Q = Heart Rate x Stroke Volume Increase heart rate
Pacing Inotropes
Increase preload Preload ≈ CVP
Increase contractility Inotropes
Decrease afterload Vasodilators
.
.
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Where were we? Our patient was having rising lactates despite minimizing O2
consumption and having normal Hgb and SaO2. As we check on him, we note that he is normotensive, warm and well-perfused, with good peripheral pulses and brisk capillary refill. He has had adequate urine output since return from the OR. What other information do you want/need?
Arterial SO2 = 100% Mixed venous SO2 = 75% Renal SO2 = 90% Cerebral SO2 = 80% CVP = 14
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So why is our lactate so high? Increased production
Dead tissue?
Decreased clearance Liver failure?
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Conclusion As the nurse is drawing a
hepatic function panel, your patient begins to seize. After terminating his seizure, an emergent head CT is performed, revealing left-sided cerebral infarction, probably a bypass-related complication.
Patient discharged to home on POD #8 on Keppra with weakness of RUE